Testing these candidates, the researchers found that three chemicals – ginkgetin, periplocin, and oleandrin – removed senescent cells without harming healthy cells. Of the three, oleandrin was found to be the most effective. All three are natural products found in traditional herbal medicines.
Oleandrin is a highly lipid-soluble cardiac glycoside isolated from the plant Nerium oleander (Apocynaceae) and is used as a traditional herbal medicine due to its excellent pharmacological properties. It is widely applied for various disease treatments, such as congestive heart failure. Recently, oleandrin has attracted widespread attention due to its extensive anti-cancer and novel anti-viral effects. However, oleandrin has a narrow therapeutic window and exhibits various toxicities, especially typical cardiotoxicity, which is often fatal.
Yeah, that one scared me off too. I used to take Ginkgo in an effort to make my brain work better (never noticed much) and did not suffer any side effects at all.
That is oleandrin, not ginkgo.
Nerium oleander , a commonly cultivated ornamental shrub of the Dogbane family
I try to use as few words as possible, sometimes not enough though.
I meant to say that the warnings on the oleander scare me from using it. I am not the least bit scared of the ginkgo, though I know it is possible to overdose on it too.
I did not know it was in the Dogbane family, that used to be a serious weed here before Roundup. BR
Last time I checked cardiac glycosides weren’t particularly broad spectrum senolytics. The paper only tests a couple of cell types, with an eye towards cancer treatment. The risk/benefit for oleandrin for aging seems almost entirely one-sided to me, so far.
You can start by looking at Yang Qi herbs and look for those which are also AMPK activators (which many if not all are).
@JuanDaw
A beautiful but poisonous flower, ‘White Oleander’ was the title of the 1999 novel by Janet Fitch. You may remember that it was made into a movie.
Non-fiction reader here. I didn’t see the movie.
My guess: rapamycin is the most effective senotherapeutic we have, and that it will reduce the number of senescent cells which develop in the first place.
This is in contrast to senolytics (which try to selectively kill senescent cells once they’ve already developed) and senomorphics (which reduce the positive-feedback spreading of senescence).
Although rapamycin’s immune-modulation may confer senomorphic properties, I believe it’s senotherapeutic properties are primarily occurring through its effect on cell size. Larger cells may be more likely to transition to senescence, in a manner independent of conventional replicative senescence.
I think a lot of substances described as senolytics are in fact Histone Deacetylase Inhibitors which cause some senescent cells to complete differentiation rather than remaining stuck in an undifferentiated state and are hence senomorphics.